Diabetes Mellitus PDF

Chapter 51 Assessment and Management of Patients With Diabetes Mellitus Diabetes Mellitus A group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both Almost 1/3 of cases are undiagnosed Prevalence is increasing Minority populations and t...

Chapter 51 Assessment and Management of Patients With Diabetes Mellitus Diabetes Mellitus A group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both Almost 1/3 of cases are undiagnosed Prevalence is increasing Minority populations and the elderly are disproportionately affected Loading… Insulin Insulin is the chief glucose regulatory hormone. Insulin is synthesized by beta cells (ß-cells) located in the islets of Langerhans in Pancreas. Insulin secretion is stimulated by Hyperglycemia Pan Islets cre (β- as cells) how does insulin work? Insulin attaches to receptors on the surface of the body’s cells Insulin acts as a “gatekeeper” for glucose, allowing it to enter cells Insulin receptor Loading… Cel l Glucose channel Glucos e  Insulin Function Insulin decreases blood glucose levels by: 1.Inhibitng glycogenolysis (Breakdown of stored glucose) in liver 2. Inhibiting gluconeogenesis (production of glucose from breaking down of amino acids and other substrates). 3. Transporting glucose into muscle, liver and adipose tissue. Muscle, liver and adipose cells require activation by insulin at insulin receptors in order to facilitate glucose transport into the cell. Neural tissue and erythrocytes do not require insulin for glucose utilization. Once glucose has entered the cell, it may be oxidized for  energy (glycolysis) or stored (glycogenesis) in the Normal physiologic insulin secretion Conceptual depiction of physiologic insulin secretion Normal prandial insulin I n s u li n le v el Adapted from Mayfield. s Breakfast Lunc Suppe Bedtim h r e Normal Basal 24-hour profile Insulin Insulin peaks immediately after meals (“prandial” insulin) There is always a base amount of insulin available (“basal” insulin) A constant supply of basal insulin is essential to maintain overall glycemic control Endogenous basal and prandial insulin secretion Basal insulin secretion Occurs continuously Suppresses hepatic glucose production between meals and overnight Maintains a nearly constant level throughout the day; therefore, it is not appropriate for handling post meal glucose increases Prandial Provides about 50% secretion insulin of daily insulin requirements Occurs in response to food intake or a meal Helps to control hyperglycemia after meals Provides the other 50% of daily insulin requirement Glucose Regulation  Classification of DM 1. Type 1 (Insulin dependent DM…..IDDM) 2. Type 2 (Non-Insulin dependent DM….NIDDM) 3. Diabetes Mellitus associated with other conditions or syndrome 4. Gestational diabetes mellitus (GDM) 5. Pre-diabetes (Impaired Glucose Homeostasis): Risk factor for DM 1. Impaired glucose tolerance(IGT) 2. Impaired fasting glycemia (IFG)) Type 1 DM (Insulin dependent DM…IDDM) Beta cells in the pancreas producing insulin are destroyed by an autoimmune process Loading… Requires insulin, as little or no insulin is produced Onset is acute and usually before 30 years of age 5–10% of persons with diabetes Causes: Type 2 Diabetes (Non-Insulin dependent DM….NIDDM) 90–95% of person with diabetes More common in persons over age 30. Causes: Insulin resistance due to obesity Impaired insulin secretion (but still there is insulin secretion Hereditary Treated initially with diet and exercise Oral hypoglycemic agents and insulin may be used DKA does not often occur in type II because there is enough insulin to prevent breakdown of fat. Pathogenesis of Type 2 Diabetes Risk factors of DM Type 1 DM: not inherited but a genetic predisposition combined with immunologic and possibly environmental (viral) factors Type 2 DM: family history of diabetes, obesity, race/ethnicity, age greater than 45 years, previous identified impaired fasting glucose or impaired glucose tolerance, hypertension ≥ 140/90, HDL ≤ 35 and/or triglycerides ≥ 250, history of gestational diabetes or babies over 9 pounds metabolic syndrome =obesity, HTN, hypercholesterolemia See Chart 41-1 Type 1 vs. Type 2 Age of onset Age of onset Usually < 30 Usually > 40 Body wt at onset Body wt at onset Normal to thin 80% overweight Insulin production Insulin production None Not enough Insulin injections Insulin injections Always Sometimes Management Management Insulin Diet (wt. Loss) Diet Exercise Exercise Possibly oral hypoglycemic meds Possibly insulin Gestational DM Occurs in about 2%–5% of all pregnancies Onset during pregnancy, usually in the second or third trimester. Causes: hormones secreted by the placenta inhibiting the action of insulin Treated with diet and, if needed, insulin to strictly maintain normal blood glucose levels Risk factors include: obesity, age older than 30 years, family history of diabetes, previous large babies (over 9 lb). Screening tests should be performed on all pregnant women between 24 and 28 weeks’ gestation. Diabetes Mellitus associated with other conditions or syndrome Accompanied by conditions known to cause DM: Pancreatic diseases Hormonal abnormalities (Cortisol and growth hormone) Medications such as corticosteroids and estrogen- containing preparations. Patient may require treatment with oral antidiabetic agents or insulin Pre-Diabetes OGTT: The oral glucose tolerance test Clinical Manifestations Three p’s (polyphagia, Polydepsia, Polyuria) Fatigue Weakness Sudden vision changes Tingling or numbness in the hands or feet Dry skin Sores that slow to heal and recurrent infection Type 1 may have sudden weight loss, nausea, vomiting, and abdominal pain if DKA has developed Clinical manifestations Onset of type 1 diabetes may be associated with sudden weight loss or nausea, vomiting, or stomach pains. Type 2 diabetes results from a slow (over years), progressive glucose intolerance and results in long- term complications if diabetes goes undetected for many years (eg, eye disease, peripheral neuropathy, peripheral vascular disease). Complications may have developed before the actual diagnosis is made Diagnostic tests Fasting plasma glucose (FPG or FBS): 126mg/dl (7.0 mmol/L) or more Random plasma glucose: more than 200mg/dl (11.1 mmol/L) plus the Symptoms of DM Oral Glucose Tolerance Test: equal to or greater than 200 mg/dl during an oral glucose tolerance test. Glycosylated Hemoglobin Assays (Hgb A1C) Charts 41-2 p 1200 & 41-3 p 1201 Fasting blood Glucose Measures blood glucose levels after fasting Results Normal: 70-100 mg/dL Prediabetic level: between 100 mg/dl and 126 mg/dl. Diabetic level: > 126 mg/dL Critical: > 400 mg/dL Critical: < 50 mg/dL Nursing Responsibilities Fast 6-8 hours before the test Water OK No insulin or anti-diabetic medications Exercise will effect results Random Plasma Glucose It is performed regardless of when the patient last ingested food. If symptoms (polydypsia, polyuria, & weight loss) are present and blood glucose levels are ≥ 200 mg/dL, there is possibility of having DM. Oral Glucose Tolerance Test The test is performed using a glucose load containing the equivalent of 75-g anhydrous glucose dissolved in water. Steps: Individual fast at least 10 hours but not more that 16 hours prior to taking this test. After the fasting plasma glucose is tested, the individual receives 75 grams of glucose in dissolved in water (100 grams for pregnant women). Blood samples are then taken at 30 minutes, 1 hour, 2 hours and 3 hours to measure glucose levels. Patient should take no medications affecting blood glucose levels. Strenuous activities should be avoided 8-12 hours prior to and during the test Diabetic level: 2hPG ≥ 200 mg/dL (2hPG is defined as two-hour postload glucose sample) When the OGTT is used the following criteria apply: 2hPG < 140 mg/dL = Normal glucose 2hPG ≥ 140 and < 200 mg/dL = Impaired Glucose Tolerance (IGT) (pre- diabetes) 2hPG ≥ 200mg/dL = provisional diagnosis of diabetes Glycosylated Hemoglobin Assays (Hgb A1C) Measuring the percentage of glycosylated hemoglobin Glucose slowly binds with Hgb glycosylated h serum glucose level h glycosylated Hgb levels Provides an average blood glucose levels Past 2-3 months Can be taken any time Normal levels: Non-diabetic level: 4-6% Diabetic level for patient with diabetes: > 7% Diabetic level for patient without diabetes: > 6.4% Type 1 & 2 Diabètes: Key Concepts Minimizing the complications of diabetes requires: Early diagnosis and treatment of diabetes Maintaining HbA1C level < 7% Achieving HbA1C < 7% requires control of post-prandial and fasting hyperglycemia  Assessment Of Diabetic patients: History: history of hypo and hyperglycemia, Glucose level, complications, Dietary compliance, and exercise. History of chronic complication Adherence to dietary, exercise, and pharmacological management plan. Physical examination: BP, WT (BMI), Check for the complications Eye, foot, skin, renal, neurological and oral examination Laboratory Examination: HgbA1c( every 3 months) Microalbuminuria or 24-hour urine collection ( annually) Fasting Lipids ( annually), serum creatinin level, and ECG Referrals to ophthalmologist and podiatry. Treatment Goal Is to Normalize insuline activity and Blood Glucose Levels Intensive control dramatically Loading… decreases vascular and neuropathic complications  Management 1. Nutritional Management 2. Exercise 3. Monitoring glucose and Ketones 4. Pharmacologic therapy 5. Education Dietary Management—Goals Provide optimal nutrition including all essential food constituents to control of total caloric intake. To maintain body wt, blood glucose level, lipid profile and B/P level in the normal range. To prevent complication. To address individual nutrition needs. To maintain the pleasure of eating. To promote a 1- to 2-pound weight loss per week, 500 to 1,000 calories are subtracted from the daily total. Role of the Nurse Be knowledgeable about dietary management Communicate important information to the dietician or other management specialists Reinforce patient understanding Support dietary and lifestyle changes Meal Planning Consider food preferences, lifestyle, usual eating times, and cultural/ethnic background Review diet history and need for weight loss, gain, or maintenance Consider caloric requirements and calorie distribution throughout the day Carbohydrates: 50% to 60% carbohydrates, emphasize whole grains Fat: 20% to 30%: No more than 10% from saturated fat, less than 300 mg cholesterol, the use of some nonanimal sources of protein (eg, legumes and whole grains) to help reduce saturated fat and cholesterol intake Fiber: Lowers total cholesterol and low-density lipoprotein cholesterol in the blood Soluble fiber (oat) improve blood glucose levels through the slower rate of glucose absorption from foods that contain this type of fiber. Insoluble fiber (whole-grain breads and cereals and in some vegetables) increase bulk of stool and prevent constipation Table 41-2 p 1204 Glycemic Index Describes how much a given food increases blood glucose Combining starchy food with protein- and fat-containing food slows absorption and glycemic response Raw or whole foods tend to have lower response than cooked, chopped, or pureed )mashed) foods Eating whole fruits rather than juices decreases the glycemic response due to fiber-slowing absorption Adding food with sugars may produce lower response if eaten with foods that are more slowly absorbed Patients can create their own glycemic index by monitoring their blood glucose level after ingesting a particular food. Other Dietary Concerns Alcohol Alcohol may inhibit gluconeogenesis hypoglycemia may develop Patient should be cautioned to eat while drinking alcohol Nutritive and non-nutritive sweeteners Acceptable for patients with diabetes Nutritive sweeteners include fructose (fruit sugar), sorbitol, and xylitol, calorie-free; provide calories similar to those in sucrose (table sugar) but cause less elevation in blood sugar. Non-nutritive sweeteners have minimal or no calories, Saccharin Reading labels Foods labeled “sugarless”, “sugar-free” or “dietetic” may provide calories Exercise Lowers blood sugar Aids in weight loss Decreases lipid profile and increases HDL Lowers cardiovascular risk Maintain a feeling of well-being (decreasing stress) Exercise Precautions Exercise when blood sugar levels are elevated (above 250 mg/dL) and ketones are present in urine should be avoided Insulin normally decreases with exercise; patients on exogenous insulin should eat a 15-g carbohydrate snack before moderate exercise to prevent hypoglycemia If exercising to control or reduce weight, insulin must be adjusted Potential exists for post exercise hypoglycemia Need to monitor blood glucose levels Exercise Recommendations Encourage regular daily exercise Gradual increase in exercise period is encouraged Modify exercise regimen to patient needs and presence of diabetic complications or potential cardiovascular problems Exercise at the same time of the day Foot care: assess, avoid trauma and proper footwear Avoid exercise in extreme heat or cold. Conduct exercise stress test for patients older than age 30 who have 2 or more risk factors is recommended Gerontologic considerations See Chart 41-5  Monitoring 1. Self-Monitoring of blood glucose( SMBG): Enables people with DM to adjust the treatment regimen to obtain optimal blood glucose control. Allow early detection of hypo and hyperglycemia and normalizing blood glucose levels. Disadvantages of SMBG are in the need for good visual acuity, fine motor coordination, cognitive ability, comfort with technology, willingness and cost Candidates for SMBG: - Unstable DM - A tendency for sever ketosis and hypoglycemia - Hypoglycemia without warning symptoms - Abnormal renal glucose threshold Frequency: 2-4 times per day is recommended (before meals and bedtime)  Cont…. 1. Glucosylated Hemoglobin: HgbA1c (2-3 month) 2. Urine testing for glucose 3. Urine testing for Ketones (Ketonuria): should be performed whenever patients with type 1 have glucosuria or persistently elevated blood glucose levels ( more than 240mg/dl for two testing periods), and during illness and pregnancy.  Pharmacological therapy. Insulin therapy Taken one or more times per day( or even more often) to control blood glucose. Accurate monitoring of blood glucose levels is essential Sources of insulin: beef, pork, and Human insulin which is now widly used Classifications: Based onset, peak, and duration of action, insulin is classified to: 1) rapid acting (lispro), 2) short acting (HR), 3) intermediat-acting (NPH or Lent), 4) Long acting (Ultralent), and 5) Mixed (70% NPH and 30% R) Insulin Types  Notices about Insulin Rapid-acting Insulin: Control the rise in glucose levels after meals, immediately after the injection. Because of rapid onset of rapid acting insulin, patients should be instructed to eat no more than 5 to 15 minutes after injection Short- acting Insulin: Control the rise in glucose levels after meals, immediately after the injection. Short acting insulin (Regular insulin) is a clear solution Usually administered 20 to 30 minutes before a meal, either alone or in combination with a longer-acting insulin Intermediate acting insulin: Control the rise in glucose levels after subsequent meals If Intermediate acting insulin (NPH or Lente insulin) is taken alone, it is not crucial that it be taken 30 minutes before the meal. Eat some food around the time of the onset and peak of these insulins Long -acting Insulin: Provide a relatively constant level of insulin and act as a basal insulin. Absorbed very slowly over 24 hours Given once a day at bedtime. Insulin glargine (Lantus) cannot be mixed with other insulins Devices definition advantages Disadvantages Insulin pen Small (150- to 300-unit) Useful for patients who have Expensive, and patient still need prefilled insulin cartridges impaired manual dexterity, vision, or to use needles that are loaded into a cognitive function due to their penlike holder difficulty of using traditional syringes or travelling Jet injection Deliver insulin through Faster delivery of insulin to blood Expensive, require training & skin under pressure( stream, No needles to be used supervision when first used, and absorbed faster) in an bruising may occur extremely fine stream. Insulin Pump Continuous s/c rapid- Increased flexibility in lifestyle (in Unexpected disruptions in the acting insulin(Lispro) terms of timing and amount of meals, flow of insulin from the pump infusion using pump, exercise, and travel) and, for many that increase the risk of DKA, delivered at a basal rate patients, improved blood glucose potential for infection at needle and as a bolus with meals. control insertion site and Hypoglycemia Implantable and Methods of administering insulin by implantable insulin pump programmed based on glucose level, the inhalant insulin oral route (oral spray or capsule), skin patch, and inhalation are undergoing intensive study Delivery. Transplantation Transplantation of the whole pancreas or a segment of the pancreas, or insulin-producing pancreatic islet cells Insulin Pump Insulin Regimen Conventional regimen: Daily dose: 1-2 injections/day (eg, one or more injections of a mixture of short- and intermediate-acting insulins per day). Purposes: 1) Avoiding acute complications of diabetes (hypoglycemia and symptomatic hyperglycemia, and 2) appropriate for the terminally ill, unwilling or unable to engage in the self-management activities that are part of amore complex insulin regimen Disadvantage: May frequently have blood glucose levels well above normal. Intensive regimen: Daily dose: 3-4 injection/day Purposes: 1) Maintaining blood glucose levels as close to normal to prevents long-term diabetic complications, and 2) allowing more flexibility to change their insulin doses in accordance with changes in their eating and activity patterns, stress and illness. Contraindications: 1) patients with nervous system disorders rendering them unaware of hypoglycemic episodes (eg, those with autonomic neuropathy), 2) recurring severe hypoglycemia, 3) irreversible diabetic complications, such as blindness or end-stage renal disease, 4) cerebrovascular and/or cardiovascular disease, and 5) Ineffective self- care skills Complications of insulin therapy Hypoglycemia: The most common complication of insulin therapy. Local allergic reaction: Swelling, redness, tenderness and induration… 2-4 cm wheal may appear in the sight of injection 1-2 hours after injection administered. (occur at the beginning stage of therapy). Systemic allergic reactions: Are rare. Can be treated with giving small doses of insulin which gradually increased. Insulin lipodystrophy: local reaction cause either lipoatrophy or lipohypertrophy (fibrofatty masses) at the site of injection. Cont… Insulin resistance: Due to obesity or immune antibodies. Morning Hyperglycemia: insufficient level of insulin due to dawn phenomena (normal glucose level up to 3 am when Bld glucose start to rise) and Somogyi effect (nocturnal hypoglycemia followed by rebound hyperglycemia) - Insulin waning: the progressive increase in blood glucose from bed time to morning and is prevented by moving the evening dose of NPH insulin to bed time Teaching Patients Insulin Self-Management Use and action of insulin Symptoms of hypoglycemia and hyperglycemia Required actions to deal with symptoms Blood glucose monitoring Self-injection of insulin: see Charts 41-7 and 41-8 Insulin pump use Alternative Methods of insulin therapy Insulin pens Jet injection: deliver insulin through skin under pressure( absorbed faster) Insulin pumps: continuous s/c insulin infusion Implantable and inhalant insulin Delivery. Transplantation. Pharmacological therapy II. Oral Antidiabetic Agents Used for patients with type 2 diabetes who cannot be treated with diet and exercise alone Combinations of oral drugs may be used Major side effects: hypoglycemia Nursing interventions: monitor blood glucose and assess for hypoglycemia and other potential side effects Patient teaching See Table 41-6 Sites of Action of Oral Antidiabetic Agents  Class Main Action Side effects Nursing consideration First-Generation Increasing insulin secretion GI symptoms, 2nd generation of this group have Sulfonylureas dermatology reactions shorter half- life than 1st Improving insulin action at the and hypoglycemia generation which make them cellular level. (most one) specially safer to use in elderly and even with delayed food in adults in regards to intake or exercise is hypoglycemia increased. Glucotrol should be taken on empty stomach Biguanides Decreasing hepatic glucose Hypoglycemia, Lactic Used in combination with output (decreasing acidosis is a potential Sulfonylureas agent glycogenolysis) serious side effect Contraindicated in patient with Facilitating insulin’s action on renal impairment or at risk for Metphormin peripheral receptors sites renal impairment (glucophage). (increased glucose uptake) renal function should be monitored, should not be administered 2 days before any diagnostic test requires use of contrast agent. Alpha Glucosidase Delaying absorption of glucose Diarrhea and flatulence Should be taken immediately Inhibitors from the intestinal system before meals. resulting in a lower postprandial blood glucose level Start with low dose, increase slowly to decrease GI effects. Cautions with liver or kidney Acarbose (Precose) Thiazolidinediones First line agent to treat type II Affect liver function LFT showed be taken as base DM, in conjunction of diet line and monthly for 12 months Can cause resumption of Enhancing insulin action at the ovulation in receptor site without increasing perimenopausal women Troglitazone insulin secretion putting them at risk for (Rezulin) pregnancy Decreasing hepatic glucose output Can cause edema and wt. gain Meglitinides Stimulate the release of insulin Hypoglycemia and wt. Take before each meal. from the pancreas gain Repaglinides (Prandin) Education The diabetic patient should be knowledgeable about: Nutrition. Medication effects, side effects and adjustment. Exercise. Disease progression and prevention strategies. Monitoring techniques. Complications of DM Acute complications: Hypoglycemia Diabetic Keto Acidosis (DKA) Hyperglycemic hyperosmolar Syndrome Chronic Complications Macrovascular complications Microvascular complications Retinopathy Nephropathy Neuropathy Hypoglycemia Blood glucose falls to less than 70 mg/dl (3.7 mmol/L) may be caused by too much medication (Insulin or hypoglycemic agents), too little food, or excessive exercise. Often occurs before meals, especially if meals are delayed or snacks are omitted, or during the peak of insulin  Manifestations of hypoglycemia The clinical manifestations of hypoglycemia represent 1) adrenergic symptoms & 2)central nervous system (CNS) symptoms. Mild hypoglycemia: Stimulation sympathetic nervous system (increased epinephrine and norepinephrine) Adrenergic symptoms: sweating, tremor, tachycardia, palpitation, nervousness, and hunger) Moderate hypoglycemia Impaired function of the CNS due to decreased fuel needed to brain cells CNS symptoms: Inability to concentrate, headache, lightheadedness, confusion, memory apses, numbness of the lips and tongue, slurred speech, impaired coordination, emotional changes, irrational behavior, double vision, and drowsiness. Sever hypoglycemia (< 40 mg/dl) CNS is so impaired CNS Symptoms: disoriented behavior, seizures, difficulty arousing from sleep, or loss of consciousness Management of hypoglycemia Immediate correction of hypoglycemia: Treating with CHO for a conscious patient: 15 gm of a fast-acting concentrated source of CHO should be given orally. Examples: 4 to 6 oz of fruit juice or regular soda or 2 to 3 teaspoons of sugar or honey The blood glucose is retested in 15 minutes after treatment and retreated if blood glucose is less than 70 to 75 mg/dL or symptoms still present. Once the symptoms resolve, a snack containing protein and starch (eg, milk or cheese and crackers) is recommended unless the patient plans to eat a regular meal or snack within 30 to 60 minutes. Initiating emergency measures for unconscious patient: Glucagon 1 mg injection: SC OR IM, onset of action 8-10 min (after 20 min regain consciousness). In hospital 25-50 ml of Dextrose 50% in water (D50%W) given IV Diabetic ketoacidosis Definition: An absence or markedly inadequate amount of insulin that result in disorder in the metabolism of CHO, protein, and fat. Mostly associated with type I DM Main clinical features are: 1. Hyperglycemia: Due to decreased glucose uptake and increased glucose production by liver. 2. Dehydration and electrolyte loss: Due to polyuria ( 6.5 L of water and up to 400-500 mEq of NA, K, CL may lost in 24 hours) 3. Metabolic Acidosis: Due to breakdown of fat into free fatty acid and glycerol. Free fatty acids converted to ketones (acids) by the liver Causes: 1. Decreased or missed dose of insulin. 2. Illness and infection(physical stressors): stimulate the secretion of stress hormones such as glucagon, epinephrine and norepinephrine, cortisol, and growth hormone….. Promote production of glucose from liver and interfere glucose utilization 3. Undiagnosed and untreated diabetes Clinical manifestations: DKA Polyuria, polydipsia and fatigue Blurred vision Weakness and headache Orthostatic hypotension due to dehydration Gastrointestinal symptoms due to acidosis: anorexia, nausea, vomiting, abd pain and acetone breath (a fruity odor). Hyperventilation (deep, not labored respiration called as Kussmaul breathing) to decrease metabolic acidosis Patient may be alert, lethargic, or comatose. Diagnostic Finding: DKA Serum glucose level vary from 300-800 mg/dl Low serum bicarbonate, low PH (6.8 to 7.3), and low PCO2 Increased ketone in blood and urine NA and K may be low, normal, or high depending on amount of water lost. Acidosis sometime increases potassium level High serum urea, creatinine and hematocrit due to dehydration Prevention of DKA Specially during illness Patient should take the usual insulin dose and additional doses prescribed for special sick day even if had nausea and vomiting Consume frequent small portion of CHO Drinking fluids every hour to prevent dehydration Assess blood glucose and urine ketones every 3-4 hrs The patient should contact health care provider if she/he can't take fluid because of vomiting or blood glucose and urine ketone still high. Medical management of DKA Rehydration to maintain tissue perfusion and enhance excretion of excessive glucose and ketones by kidney. May need 6-10 L: N/S.9% initially started with high rate and may be replaced with N/S.45% Rehydration leads to increased plasma volume and decreased K+, insulin enhances the movement of K+ from extracellular fluid into the cells Restoring electrolytes mainly potassium. Treat acidosis: IVF (normal saline) to wash out Ketones Insulin infusion ( 5unit/hr) to inhibit new formation of ketones Bicarbonate infusion is contraindicated because causing sever sudden hypokalemia Nursing Management: DKA Carrying medical orders Assessment: V/S Serum glucose and urine ketone level Serum potassium level ABG’s I&O ECG due to effect of Hpo or hyperkalemia on heart. Respiratory assessment Neurological assessment Hyperglycemic hyperosmolar Syndrome (HHS) Hyperglycemia, hyperosmolarity present, and alteration of awareness, with ketonsis is minimal or absent. Causes or Risk factors: Lack of effective insulin ( insulin resistance)… TYPE II DM. Elderly patients (50 years old or older) with mild type 2 DM. Elderly patients with no known history of diabetes Acute illness (eg, pneumonia, cerebrovascular accident [CVA]) Medications (eg, thiazides) that exacerbate hyperglycemia. Hypokalemia interfere with the transport of glucose into the cell as well as inhibit insulin secretion in the pancreas Pathophysiology: HHS Persistent hyperglycemia causes osmotic diuresis, resulting in losses of water and electrolyte With glycosuria and dehydration, hypernatremia and increased osmolality occur. Hyperglycemia and dehydration may be more sever. Clinical manifestation: hypotension, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, alteration in awareness, hemiparesis Assessment and Diagnostic findings: HHS High blood glucose (600-1200) Serum electrolyte imbalance Increased BUN creatinine Serum osmolality (> 350 mOsm/kg). Neurologic signs (eg, seizures and hemiparesis). Postural hypotension due to dehydration Management: HHS Fluid replacement Started with 0.9% or 0.45% NS, depending on the patient’s sodium level and the severity of volume depletion Replacement IV fluids with dextrose are administered (as in DKA) when the glucose level is decreased to the range of 250 to 300 mg/dL (13.8 to 16.6 mmol/L) Correction of electrolyte imbalance Potassium may be added to IV fluids Insulin administration Insulin has a less important role in the treatment of HHNS because it is not needed for reversal of acidosis, as in DKA. Extremely elevated blood glucose levels drop as the patient is rehydrated insulin is usually administered at a continuous low rate to treat hyperglycemia Retinopathy Definition: Deterioration of the small blood vessels that nourish the retina Stages: Background: Asymptomatic retinopathy. Blood vessels within the retina develop microaneurysms that leak fluid, causing swelling and forming deposits (exudates). In some cases, macular edema causes distorted vision Preproliferative: Represents increased destruction of retinal blood vessels Proliferative: Abnormal growth of new blood vessels on the retina. New vessels rupture, bleeding into the vitreous and blocking light. Ruptured blood vessels in the vitreous form scar tissue, which can pull on and detach the retina. C/M: painless, blurred vision due to macular edema, hemorrhage may not cause symptoms or sometimes causes floaters or cobwebs in the visual field, or sudden visual changes including spotty or hazy vision, or complete loss of vision. Management: Prevention: Managing hyperglycemia Treatment: Argon laser photocoagulation that destroys leaking blood vessels and areas of neovascularization Nephropathy Definition: Renal disease secondary to diabetic microvascular changes in the kidney Pathophysiology: when blood glucose levels are elevated, the kidney’s filtration mechanism is stressed, allowing blood proteins to leak into the urine. As a result, the pressure in the blood vessels of the kidney increases. The elevated pressure serves as the stimulus for the development of nephropathy. Diagnostic test: Microalbuminurea: microalbuminuria is  discovered in a 24-hour urine sample, urine Neuropathy Definition: a group of diseases that affect all types of nerves, including peripheral (sensorimotor), autonomic, and spinal nerves Capillary basement membrane thickening and capillary and demyelinization of the nerves, which is thought to be related to hyperglycemia. Pathophysiology: Neuropathy The two common types of diabetic neuropathy: Peripheral neuropathy: Affects the distal portions of the nerves, especially the nerves of the lower extremities. C/M: Paresthesia (prickling, tingling, or heightened sensation), burning sensations (especially at night), Decreased sensations of pain and temperature, decrease in deep tendon reflexes and vibratory sensation, foot and joint deformities. Autonomic neuropathy: Neuropathy of the autonomic nervous system results in a broad range of dysfunctions affecting almost every organ system of the body. Cardiac: Tachycardic; orthostatic hypotension; and silent, or painless, myocardial ischemia and infarction GI: Delayed gastric emptying may occur with the typical symptoms of early satiety, bloating, nausea, and vomiting, diabetic constipation or diarrhea Renal systems: Urinary retention due a decreased sensation of bladder fullness, UTI Endocrine: Diminished or absent adrenergic symptoms of hypoglycemia due to autonomic neuropathy of the adrenal medulla, decrease or absence of sweating Management of Neuropathy Prevention: Control of blood glucose level Management strategies depend on the symptoms Orthostatic hypotension: A diet high in sodium Delayed gastric emptying: a low-fat diet, frequent small meals, and use of agents that increase gastric motility (eg, metoclopramide, bethanechol). Diabetic diarrhea: antidiarrheal agents. Constipation: A high-fiber diet, adequate hydration, laxatives, and enemas. Skin dryness: lotion, educations about skin care and heat intolerance Macro vascular Complications MACROVASCULAR COMPLICATIONS: Coronary artery disease Cerebrovascular disease Peripheral vascular disease Pathophysiology: Blood vessel walls thicken Sclerose, and become occluded by plaque that adheres to the vessel walls Eventually, blood flow is blocked One unique feature of coronary artery disease in patients with diabetes is that the typical ischemic symptoms may be absent.  Diabetic foot Three diabetic complications increase risk of Diabetic foot: 1. Neuropathy: Peripheral neuropathy leads to loss of pain and pressure sensation, autonomic neuropathy lead to increase dryness and fissuring of the skin 2. Peripheral vascular disease: poor circulation…. Poor wound healing 3. Immunocompramise: DM impairs the ability of specialized WBC’s to destroy bacteria. Initial C/M: Drainage, swelling, redness (from cellulitis) of the leg, or gangrene. High risks for Diabetic foot Duration of DM more than 10 years. Age greater than 40 years. Current smoker and history of smoking. Decreased peripheral pulses Decreased sensation Anatomical deformities and pressure areas. History of previous foot ulcers or amputation. Management of Diabetic foot Prevention: Teaching patients proper foot care daily assessment of feet for any redness, blisters, fissures, calluses, ulcerations, and changes in skin temperature use of a mirror to inspect the bottom of the feet or the help of a family member in foot inspection interior surfaces of shoes should be inspected for any rough spots or foreign objects Properly bathing, drying, and lubricating the feet, Wearing closed-toe shoes fitting well Trimming toenails straight Avoiding home remedies or over-the-counter agents or self-medicating to treat foot problems, managing hyperglycemia. Treatment: Bed rest, antibiotics, and débridement  Nursing diagnosis of newly diagnosed with DM 1. Risk for fluid volume deficit related to polyuria and dehydration 2. Altered nutrition related to imbalance of insulin, food and physical activity 3. Knowledge deficit about diabetes self- care skills 4. Potential self-care deficit related to physical impairment or social factors 5. Anxiety related to loss of control, fear of inability to manage diabetes